Search results for "interleukin-1"

showing 10 items of 660 documents

Induction of regulatory Tr1 cells and inhibition of TH17 cells by IL-27

2011

Accumulating evidence indicates that IL-27, a member of the IL-12 family of cytokines, alleviates the severity of autoimmune diseases in both mice and men. The IL-27-induced activation of signal transducer and activator of transcription (Stat)1 and Stat3 promotes the generation of IL-10- producing type 1 regulatory T (Tr1) cells that inhibit effector T cells. In addition, IL-27 also suppresses the development of pathogenic IL-17-producing CD4(+) T cells (T(H)17) cells suggesting that pharmacological manipulations of IL-27 signaling pathway could be exploited therapeutically in regulating tissue inflammation. Here, we review how IL-27 controls inflammation through the regulation of Tr1 and T…

Interleukins/immunologyImmunologyInterleukin-10/biosynthesis/immunologyT-Lymphocytes Regulatory/immunologyddc:616.07T-Lymphocytes RegulatoryArticleAutoimmune Diseases03 medical and health sciences0302 clinical medicineImmunology and AllergyCytotoxic T cellTh17 Cells/immunologyAnimalsHumansIL-2 receptorSTAT3STAT4030304 developmental biology0303 health sciencesbiologyZAP70InterleukinsFOXP33. Good healthCell biologyddc:616.8Interleukin-10Interleukin 10Autoimmune Diseases/immunologyImmunologyInterleukin 12biology.proteinTh17 Cells030215 immunology
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Potassium regulates IL-1 beta processing via calcium-independent phospholipase A2.

2000

Abstract We report that potassium leakage from cells leads to activation of the Ca2+-independent phospholipase A2 (iPLA2), and the latter plays a pivotal role in regulating the cleavage of pro-IL-1β by the IL-converting enzyme caspase-1 in human monocytes. K+ efflux led to increases of cellular levels of glycerophosphocholine, an unambiguous indicator of phospholipase A2 activation. Both maturation of IL-1β and formation of glycerophosphocholine were blocked by bromoenol lactone, the specific iPLA2 inhibitor. Bromoenol lactone-dependent inhibition of IL-1β processing was not due to perturbation of the export machinery for pro-IL-1β and IL-1β or to caspase-1 suppression. Conspicuously, activ…

Intracellular FluidPotassiumImmunologychemistry.chemical_elementNaphthalenesCleavage (embryo)MonocytesPhospholipases APhospholipase A2Calcium-Independent Phospholipase A2Immunology and AllergyHumansCells Culturedchemistry.chemical_classificationCalcium metabolismbiologyTumor Necrosis Factor-alphaCaspase 1Biological TransportCaspase InhibitorsCell biologyEnzyme ActivationPhospholipases A2EnzymechemistryPyronesbiology.proteinPotassiumCalciumEffluxBromoenol lactoneProtein Processing Post-TranslationalImmunosuppressive AgentsInterleukin-1Journal of immunology (Baltimore, Md. : 1950)
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Kalanchoe pinnata inhibits mast cell activation and prevents allergic airway disease

2011

Aqueous extract of Kalanchoe pinnata (Kp) have been found effective in models to reduce acute anaphylactic reactions. In the present study, we investigate the effect of Kp and the flavonoid quercetin (QE) and quercitrin (QI) on mast cell activation in vitro and in a model of allergic airway disease in vivo. Treatment with Kp and QE in vitro inhibited degranulation and cytokine production of bone marrow-derived mast cells following IgE/FcɛRI crosslinking, whereas treatment with QI had no effect. Similarly, in vivo treatment with Kp and QE decreased development of airway hyperresponsiveness, airway inflammation, goblet cell metaplasia and production of IL-5, IL-13 and TNF. In contrast, treatm…

KalanchoeOvalbuminmedicine.medical_treatmentBasophil Degranulation TestPharmaceutical ScienceInflammationImmunoglobulin EMiceIn vivoDrug DiscoverymedicineAnimalsMast CellsPharmacologyMetaplasiaMice Inbred BALB CGoblet cellInterleukin-13biologyPlant ExtractsTumor Necrosis Factor-alphabusiness.industryDegranulationIn vitroCytokinemedicine.anatomical_structureComplementary and alternative medicineImmunologybiology.proteinMolecular MedicineQuercetinTumor necrosis factor alphaGoblet CellsBronchial HyperreactivityInterleukin-5medicine.symptombusinessPhytotherapyPhytomedicine
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Keratinocytes Determine Th1 Immunity during Early Experimental Leishmaniasis

2010

Experimental leishmaniasis is an excellent model system for analyzing Th1/Th2 differentiation. Resistance to Leishmania (L.) major depends on the development of a L. major specific Th1 response, while Th2 differentiation results in susceptibility. There is growing evidence that the microenvironment of the early affected tissue delivers the initial triggers for Th-cell differentiation. To analyze this we studied differential gene expression in infected skin of resistant and susceptible mice 16h after parasite inoculation. Employing microarray technology, bioinformatics, laser-microdissection and in-situ-hybridization we found that the epidermis was the major source of immunomodulatory mediat…

KeratinocytesCellular differentiationImmunology/Innate ImmunityInterleukin-1betaGene ExpressionInfectious Diseases/Skin InfectionsMiceT-Lymphocyte SubsetsLeishmania majorBiology (General)In Situ HybridizationOligonucleotide Array Sequence AnalysisSkinRegulation of gene expressionMice Inbred BALB CReverse Transcriptase Polymerase Chain ReactionCell DifferentiationImmunohistochemistryInterleukin-12MicrodissectionResearch ArticleQH301-705.5ImmunologyLeishmaniasis CutaneousBiologyMicrobiologyTh2 CellsImmune systemCutaneous leishmaniasisImmunology/Immunity to InfectionsVirologyGeneticsmedicineAnimalsDermatology/Skin InfectionsMolecular BiologyInterleukin 4Epidermis (botany)Interleukin-6Gene Expression ProfilingLasersTh1 CellsRC581-607medicine.diseasebiology.organism_classificationMice Inbred C57BLGene expression profilingDisease Models AnimalImmunology/Immune ResponseImmunologyOsteopontinParasitologyInterleukin-4Immunologic diseases. AllergyPLoS Pathogens
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Epidermal Cells Enhance Interleukin 4 and Immunoglobulin E Production After Stimulation with Protein Allergen

1996

Exposure to certain allergens via epithelial tissues is the primary route for tile induction of immunoglobulin E–dependent allergies of the immediate type associated with atopic diseases. In order to address the question whether and how epithelial cells might contribute to the induction or increase of T H2 -dependent IgE production, we performed co-culture experiments of syngeneic epidermal cells and cells from the associated lymphoid tissue or spleen (responder cells) of BALB/c mice primed with ovalbumin in vivo . In the presence of ovalbumin in vitro , immunoglobulin E but not immunoglobulin G 2a production was significantly enhanced by the addition of epidermal cells, and separation of e…

KeratinocytesLymphoid TissueOvalbuminDermatologyMajor histocompatibility complexImmunoglobulin EBiochemistryImmunoglobulin GMiceAntigenAnimalsRNA MessengerMolecular BiologyInterleukin 4Mice Inbred BALB CDose-Response Relationship Drugintegumentary systembiologyHistocompatibility Antigens Class IIDendritic CellsCell BiologyAllergensImmunoglobulin EMolecular biologycytokinesInterleukin-10Raji cellInterleukin 10Epidermal CellsLangerhans CellsIL-10biology.proteinFemaleImmunizationInterleukin-4EpidermisAntibodyJournal of Investigative Dermatology
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Imiquimod-Induced Psoriasis in Mice Depends on the IL-17 Signaling of Keratinocytes

2018

The pathology of psoriasis strongly depends on IL-17A. Monoclonal antibodies blocking either the cytokine or its receptor are among the most efficient treatments for psoriatic patients. Keratinocytes can be activated upon exposure to IL-17A and tumor necrosis factor-α and secrete secondary cytokines and chemokines in the inflamed skin. In psoriasis and its imiquimod-induced mouse model, a strong skin infiltration of neutrophils and inflammatory monocytes can be observed. However, to date, it is not clear how exactly those cellular populations are attracted to the skin and how they contribute to the pathogenesis of the disease. To define the crucial cell type responding to IL-17 and initiati…

KeratinocytesMale0301 basic medicineCell typeChemokinemedicine.medical_treatmentImiquimodDermatologyReal-Time Polymerase Chain ReactionBiochemistryMiceRandom Allocation03 medical and health sciences0302 clinical medicineAdjuvants ImmunologicPsoriasismedicineAnimalsPsoriasisMolecular BiologyCells CulturedImiquimodbiologyTumor Necrosis Factor-alphabusiness.industryBiopsy NeedleInterleukin-17Cell BiologyFlow Cytometrymedicine.diseaseImmunohistochemistryMice Inbred C57BLDisease Models Animal030104 developmental biologyCytokinemedicine.anatomical_structure030220 oncology & carcinogenesisImmunologybiology.proteinCytokinesFemaleTumor necrosis factor alphaInterleukin 17KeratinocytebusinessSignal Transductionmedicine.drugJournal of Investigative Dermatology
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Epigenetic control of IL-23 expression in keratinocytes is important for chronic skin inflammation

2018

The chronic skin inflammation psoriasis is crucially dependent on the IL-23/IL-17 cytokine axis. Although IL-23 is expressed by psoriatic keratinocytes and immune cells, only the immune cell-derived IL-23 is believed to be disease relevant. Here we use a genetic mouse model to show that keratinocyte-produced IL-23 is sufficient to cause a chronic skin inflammation with an IL-17 profile. Furthermore, we reveal a cell-autonomous nuclear function for the actin polymerizing molecule N-WASP, which controls IL-23 expression in keratinocytes by regulating the degradation of the histone methyltransferases G9a and GLP, and H3K9 dimethylation of the IL-23 promoter. This mechanism mediates the inducti…

KeratinocytesMale0301 basic medicinemedicine.medical_treatmentWiskott-Aldrich Syndrome Protein NeuronalGeneral Physics and AstronomyEpigenesis GeneticHistonesMice0302 clinical medicineGenes ReporterInterleukin 23Promoter Regions Geneticlcsh:ScienceSkinMice KnockoutMultidisciplinaryInterleukin-17QMiddle AgedCytokine030220 oncology & carcinogenesisHistone methyltransferaseTumor necrosis factor alphaSignal transductionmedicine.symptomSignal TransductionAdultScienceGreen Fluorescent ProteinsPrimary Cell CultureInflammationBiologyArticleGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesImmune systemPsoriasismedicineAnimalsHumansPsoriasisInflammationHistone-Lysine N-MethyltransferaseGeneral Chemistrybiochemical phenomena metabolism and nutritionmedicine.diseaseDisease Models AnimalHEK293 Cells030104 developmental biologyInterleukin-23 Subunit p19Cancer researchlcsh:QNature Communications
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In contrast to their murine counterparts, normal human keratinocytes and human epidermoid cell lines A431 and HaCaT fail to express IL-10 mRNA and pr…

1997

Abstract In mice, keratinocyte-derived IL-10 is up-regulated by ultraviolet-B (UVB) radiation and plays a major role in UVB-induced immunosuppression. The present study was designed to examine whether a comparable phenomenon can be detected in man. Freshly isolated or cultured normal human keratinocytes (NHK) and keratinocyte cell lines A431 and HaCaT were stimulated with graded doses of UVB (up to 200 J/m2) or with a variety of other stimuli. RNA was extracted at various time points post-stimulation and analysed by reverse transcriptase-polymerase chain reaction (RT-PCR) using four different IL-10-specific primer pairs and RNA from monocytes or T cells as positive controls. We failed to de…

KeratinocytesMaleCell typeUltraviolet Raysmedicine.medical_treatmentImmunologyBiologyMelanocyteEpitheliumMicemedicineTumor Cells CulturedImmunology and AllergyAnimalsHumansRNA MessengerMessenger RNAEpidermis (botany)integumentary systemOriginal ArticlesInterleukin-10HaCaTCytokinemedicine.anatomical_structureCell cultureImmunologyMelanocytesKeratinocyteClinical and experimental immunology
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Induction of inflammatory cytokines in murine keratinocytes upon in vivo stimulation with contact sensitizers and tolerizing analogues

1992

In order to elucidate the role of keratinocytes (KCs) in the induction of contact sensitivity, we applied various contact sensitizers [2,4-dinitrofluorobenzene (DNFB), urushiol, 3-n-pentadecylcatechol (PDC), 4-ethoxymethylene-2-phenyloxazol-5-one (oxazolone)] and tolerizing compounds [2,4-dinitrothiocyanobenzene (DNTB), 5-methyl-3-n-pentadecyl-catechol (5-Me-PDC)] onto the earskin of non-sensitized Balb/c mice. In addition, we applied croton oil as a non-sensitizing, but stimulatory agent. Cytokine production was demonstrated by Northern blot hybridization of the total cellular RNA extracted from epidermal cells depleted by Langerhans cells and Thy 1+ dendritic cells using radiolabeled DNA …

Keratinocytesmedicine.medical_treatmentAlpha (ethology)DermatologyBiologyDermatitis ContactBiochemistryProinflammatory cytokineMiceIn vivomedicineAnimalsCroton oilRNA MessengerMicroscopy ImmunoelectronMolecular BiologyCells CulturedMice Inbred BALB CEpidermis (botany)Tumor Necrosis Factor-alphaEarBlotting NorthernImmunohistochemistryMolecular biologyStimulation ChemicalTolerance inductionCytokineImmunologyCytokinesTumor necrosis factor alphaInterleukin-1Experimental Dermatology
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Distinct Roles for IL-1 Receptor Type I Signaling in Early Versus Established Leishmania major Infections

2006

IL-1alpha/beta released by infected dendritic cells (DC) plays a critical role in the development of protective immunity against Leishmania major. Previous studies demonstrated that treatment of susceptible BALB/c mice with IL-1alpha during T-cell priming (days 1-3 post-infection) induced T helper (Th)1-mediated protection. In contrast, we now demonstrate that prolonged treatment with IL-1alpha (for 3 weeks) worsened disease outcome. To characterize the receptor involved, L. major infections in IL-1 receptor type I (IL-1RI) knockout mice were studied. In C57BL/6 IL-1RI-/- mice, the IL-1alpha-mediated protective effect was abrogated. The course of high-dose infection (2 x 10(5) parasites) in…

Leishmaniasis CutaneousPriming (immunology)DermatologyReceptor typeBiochemistryInterferon-gammaMiceTh2 CellsmedicineAnimalsParasite hostingLeishmania majorL-SelectinReceptorMolecular BiologyLeishmania majorMice KnockoutReceptors Interleukin-1 Type IMice Inbred BALB CbiologyReceptors Interleukin-1LeishmaniasisT-Lymphocytes Helper-InducerCell BiologyTh1 Cellsbiology.organism_classificationmedicine.diseaseMice Inbred C57BLGene Expression RegulationCD4 AntigensImmunologyKnockout mouseDisease ProgressionInterleukin-4Ex vivoInterleukin-1Signal TransductionJournal of Investigative Dermatology
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